Pathak Sanket, Conermann Till
Allegheny Health Network
Low back pain is a common cause of disability among the general population, with a well-documented cost burden placed on the U.S. healthcare system. There are multiple sources of chronic low back pain, often divided into whether the pain is facet-mediated, myofascial, herniation-related, secondary to fracture, or discogenic in nature. This article will focus on the pathophysiology, evaluation, and treatment of lumbosacral discogenic syndrome and pain arising from intervertebral disc pathology. Intervertebral discs are pads of fibrocartilage that sit between the spinal vertebrae, occupying roughly one-third of the height of the spinal column. Their primary role is transmitting mechanical loading from body weight and muscle activity, allowing bending, flexion, and torsion of the bony spine. Each disc has two main components: a central, gel-like substance called the nucleus pulposus and an outer, firmer annulus fibrosis. The consistency of the nucleus is due to its water and proteoglycan content and is held together by a network of type II collagen and elastin fibers. This network's high anionic glycosaminoglycan content gives the nucleus pulposus its osmotic properties, allowing it to resist compression. The annulus fibrosis comprises bundles of type I collagen arranged in multiple oblique layers called lamellae. Characteristics of a normal, healthy disc demonstrate high water content in the nucleus and inner annulus. The outermost annulus provides tensile strength. A healthy disc is typically 7 to 10 mm thick and 4 cm in diameter in the lumbar region, with approximately 20 layers of lamellae. The sinuvertebral nerve (SVN) supplies the interverbal discs, which innervates the posterior annulus and posterior longitudinal ligament. In healthy subjects, the neural penetration of the annulus is about 3 mm, corresponding to the outer three lamellae. It is a mixed nerve containing a somatic root from the ventral ramus and an autonomic root from the grey ramus. Once the nerve takes a recurrent course through the intervertebral foramen and enters the spinal canal, it divides into superficial and deep networks. The superficial network branches to multiple vertebral levels and contains mostly sympathetic fibers, while the deep network contains primarily somatic fibers and innervates the corresponding segment. The intervertebral discs are relatively avascular, with the nucleus and inner annulus being supplied by capillaries that arise in the vertebral bodies and terminate at the bone-disc junction. Nutrients and small molecules such as glucose and oxygen reach the disc cells by diffusion. Additionally, only the outermost portion of the annulus is vascularized. As a result, intervertebral discs are very limited in their ability to heal from injury, and degenerative changes overtake the healing process. This is not just due to avascularity but also to a decreased cell population, which diminishes the structure's ability to break down and turn over large collagen bundles. Axial back pain may be of discogenic origin. However, not all damaged or degenerated discs cause pain. Disc abnormalities are commonly seen on MRI in asymptomatic individuals. Considering other possible axial low back pain etiologies with similar clinical presentation, this presents a challenge to the treatment provider.
下腰痛是普通人群致残的常见原因,美国医疗保健系统为此承受着有据可查的成本负担。慢性下腰痛有多种成因,通常根据疼痛是否由小关节介导、肌筋膜性、与椎间盘突出相关、继发于骨折或本质上是椎间盘源性来划分。本文将重点探讨腰骶部椎间盘源性综合征的病理生理学、评估和治疗,以及由椎间盘病变引起的疼痛。椎间盘是位于脊椎之间的纤维软骨垫,约占脊柱高度的三分之一。其主要作用是传递来自体重和肌肉活动的机械负荷,使骨性脊柱能够弯曲、屈伸和扭转。每个椎间盘有两个主要组成部分:中央的凝胶状物质,称为髓核;以及外部较硬的纤维环。髓核的稠度归因于其水和蛋白聚糖含量,并由II型胶原蛋白和弹性纤维网络维系在一起。该网络中高含量的阴离子糖胺聚糖赋予髓核渗透特性,使其能够抵抗压缩。纤维环由I型胶原束组成,排列成多个称为板层的斜层。正常健康椎间盘的特征是髓核和纤维环内层含水量高。最外层纤维环提供抗张强度。健康的腰椎间盘通常厚7至10毫米,直径4厘米,约有20层板层。窦椎神经为椎间盘供血,支配纤维环后部和后纵韧带。在健康受试者中,神经穿入纤维环的深度约为3毫米,对应于外侧三层板层。它是一条混合神经,包含来自腹侧支的躯体根和来自灰交通支的自主根。一旦神经经椎间孔折返并进入椎管,它就会分成浅支和深支网络。浅支网络分支至多个椎体节段,主要包含交感神经纤维,而深支网络主要包含躯体纤维,支配相应节段。椎间盘相对无血管,髓核和纤维环内层由起源于椎体并止于骨 - 椎间盘交界处的毛细血管供血。营养物质和葡萄糖、氧气等小分子通过扩散到达椎间盘细胞。此外,只有纤维环的最外层有血管供应。因此,椎间盘从损伤中愈合的能力非常有限,退行性变超过了愈合过程。这不仅是由于无血管性,还由于细胞数量减少,这降低了结构分解和更新大胶原束的能力。轴向背痛可能源于椎间盘源性。然而,并非所有受损或退变的椎间盘都会引起疼痛。在无症状个体的MRI上通常也能看到椎间盘异常。考虑到其他可能具有相似临床表现的轴向性下腰痛病因,这给治疗提供者带来了挑战。